Figure 3

Hoechst-IGF1 preserves cardiac function and attenuates cardiac fibrosis following MI.

(A) Representative echocardiographic M-mode images and bar graph depicting cardiac contractility at 28 days following IR. As shown, H-IGF1 treated mice demonstrated greater percent fractional shortening than PBS and S-IGF1 treated mice (%FS, mean ± SEM: 41.55 ± 2.49 vs. 29.18 ± 3.51 vs. 27.83 ± 1.06). * p < 0.01 vs. S-IGF1, ** p < 0.001 vs. PBS, n = 5–9 per group, one-way ANOVA followed by Tukey's post-test. (B–D) Invasive cardiac hemodynamic measurements determined at 28 days following IR. H-IGF1 treatment led to significantly improved (B) Ejection fraction and (C) End-diastolic volumes compared to PBS and S-IGF1 treated mice. (D) End-systolic volumes were not different between sham and H-IGF1 treated mice (n = 5 per group, *p < 0.05 vs. sham mice, ^# p < 0.05 vs. S-IGF1 treated mice, one-way ANOVA followed by Tukey's post-test). (E) Representative Picrosirius red images from histologic sections of hearts from PBS, S-IGF1 and H-IGF1 treated mice. Black scale bar represents 1 mm. H-IGF1 treatment reduced collagen content in the left ventricle compared to PBS treated mice (n = 5–6 per group, *, p < 0.05 vs. PBS, one-way ANOVA followed by Tukey's post-test).